摘要
为了探讨胆囊收缩素 (CCK)受体在中枢神经系统中的信号传递机制 ,观察了CCK8和CCKA 受体拮抗剂L 36 4,718、CCKB 受体拮抗剂L 36 5 ,2 6 0对大鼠大脑皮质钙调素 (CaM )活性的影响 .结果表明 :a CCK8对CaM活性的影响具有时间依赖性 ,15min达到最高点后逐渐下降 ;b CCK8在 10 -12 ～ 10 -7mol/L范围内可刺激CaM活性的增加 ,超过 10 -7mol/L后 ,逐渐趋于饱和 .c CCKA 受体拮抗剂L 36 4,718、CCKB 受体拮抗剂L 36 5 ,2 6 0均可抑制 10 -7mol/LCCK8引起的CaM活性的增加 ,但两者IC50 相差 40倍 ,L 36 5 ,2 6 0在较低浓度时即能明显拮抗CCK8引起的CaM活性变化 .研究结果提示CCK8可能通过CCKB 受体引起CaM活性变化 ,而CaM可能是CCKB
In order to investigate the effects of cholecystokinin octapeptide(CCK 8) on calmodulin activity in rat cerebral cortex,the cerebral cortex neurocytes was used as a model. CCK 8 stimulated the activation of CaM in a time dependent manner. After 15 minutes of treatment of 1 μmol/L CCK 8,the CaM activity reached the maximum increase. CaM activity was increased in a dose dependent manner by CCK 8 (10 -12 ～10 -7 mol/L). The CCK B specific receptor antagonist L 365,260 and with a weaker efficiency,the CCK A specific receptor antagonist L 364,718,were able to block a maximal effect of CCK 8 induced CaM activation,suggesting that CCK B receptor may regulate CaM activity in cerebral cortex.
出处
《生物化学与生物物理进展》
SCIE
CAS
CSCD
北大核心
2000年第5期533-536,共4页
Progress In Biochemistry and Biophysics
